Nitric oxide synthase inhibitors are known to increase pulmonary vasomotor tone and potentiate hypoxic vasoconstriction (HV) in the neonatal pig lung, suggesting that nitric oxide (NO) production is involved in the maintenance of basal pulmonary vasomotor tone and modulates the HV response. To determine the impact of hypoxia on endogenous pulmonary NO production, we studied 4 groups of isolated neonatal pig lungs. In 3 groups, the accumulation of nitrite+nitrate (NOx) was measured in the recirculating perfusate. Control lungs were ventilated with gas containing 16% O2. Hypoxic lungs were ventilated with gas containing 7% O2, and Nω-nitro-L-arginine methylester (NAME) lungs were ventilated with the control gas with NAME added. In a fourth group of lungs, exhaled NO (eNO) production was measured during control and hypoxia and with NAME added. Control lungs had a stable perfusion pressure (Pa - Pv), and both hypoxia and NAME increased Pa - Pv. The results given in the table(mean ± SE, nmol/min, * p<0.05 compared to control) suggest that under control conditions there was continuous production of NO, that was decreased by hypoxia or NAME. The potentiation of HV by NO inhibitors and the attenuation of NO production by hypoxia leaves a paradox that remains to be resolved. Supported by American Heart Association and Dept of VA.

Table 1
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